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        Synergic adsorption of acid blue 80 and heavy metal ions (Cu2+/Ni2+) onto activated carbon and its mechanisms

        Xinsheng Luo,Ziqiang Lei,Pengxin Zhou,Yani Liu,Guofu Maa,Zhe Zhang 한국공업화학회 2015 Journal of Industrial and Engineering Chemistry Vol.27 No.-

        A novel synergic adsorption process of acid blue 80 dye (AB80) and heavy metal ions (Cu2+ or Ni2+) on alow-cost activated carbon (PRAC) which was prepared from potato residue was reported. The resultsindicated that the maximum adsorption capacity of PRAC for AB80 and Cu2+ were 294.7 mg/g and45.0 mg/g in the AB80-Cu2+ system, respectively. In the mono-component system, the values were173.0 mg/g and 26.8 mg/g, respectively. Compared with mono-component system, the AB80 and Cu2+showed good synergistic effect on PRAC. The similarly result was revealed in the AB80-Ni2+ system. For abinary system, the adsorption isotherm of AB80 and heavy metal ions followed the non-modified Sipsmodel, and the adsorption kinetic models followed the pseudo-second order kinetic model. The effect ofpH also was discussed, and showed significant role in the binary-component system adsorption. Theselectivity in synergic adsorption was discussed. BET, FE-SEM/EDX and XPS were used to characterizePRAC with and without adsorbed dye and heavy metal ions, possible mechanisms of AB80 and heavymetal ions synergic adsorption process were proposed.

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        A20 ameliorates disc degeneration by suppressing mTOR/BNIP3 axis-mediated mitophagy

        Peng Xin,Zhang Cong,Gao Jia-Wei,Wang Feng,Bao Jun-Ping,Zhou Zhi-Min,Sun Rui,Ji Hang-Yu,VLF Cabral,Wu Xiao-Tao 한국유전학회 2023 Genes & Genomics Vol.45 No.5

        Background The pathological mechanism of intervertebral disc degeneration (IDD) is an unanswered question that we are committed to exploring. A20 is an anti-inflammatory protein of nucleus pulposus (NP) cells and plays a protective role in intervertebral disc degeneration. Objective This study aims to investigate the molecular mechanism by which A20 attenuates disc degeneration. Methods The proteins of interest were measured by immunoblotting, immunofluorescence, ELISA assay, and immunohistochemical technique to conduct related experiments. Immunofluorescence assays and mitochondrial membrane potential (JC-1) were used to assess mitophagy and mitochondrial fitness, respectively. Results Here, we demonstrated that A20 promoted mitophagy, attenuated pyroptosis, and inhibited the degradation of the extracellular matrix, consequently significantly ameliorating disc degeneration. Mechanistically, A20 reduces pyroptosis and further suppresses cellular mTOR activity. On the one hand, A20-induced mTOR inhibition triggers BNIP3-mediated mitophagy to ensure mitochondrial fitness under LPS stimulation, as a result of mitigating mitochondrial dysfunction induced by LPS. On the other hand, A20-induced mTOR inhibition reduces the loss of mitochondrial membrane potential and the generation of Mitochondrial ROS. Conclusion The study revealed that A20 promotes BNIP3-mediated mitophagy by suppressing mTOR pathway activation against LPS-induced pyroptosis.

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